Indications
Water constitutes about 60% of the average adult body weight and is responsible for many physiological processes in the human body. Thus, fluid and electrolyte homeostasis is critical for human survival, as exemplified by the potentially devastating consequences of fluid imbalance. The balance of total body fluid is an extremely well-regulated process that ensures the maintenance of a balance between fluid gain and loss through different physiological mechanisms such as neural regulation of thirst, hormonal regulation (vasopressin and natriuretic peptides), management through the skin, hemodynamic changes, and renal control of salt and water excretion. In particular, renal excretion of urine also ensures the elimination of products of metabolic activity and excess electrolytes in addition to water, thus maintaining fluid homeostasis. Fluid balance so inextricably links with electrolyte balance both in the intracellular (rich in K+ ions) and extracellular (rich in Na+ & Cl- ions) compartments, that unsurprisingly, trading of electrolytes is the core strategy of renal fluid regulation. Drugs that affect renal regulation of electrolyte excretion have the greatest effect in terms of the quantity of fluid control and thus water homeostasis.[1][2][3]
Diuretics are drugs that pharmacologically tilt the renal fluid regulation in favor of the excretion of water and electrolytes. Thus, diuretics are substances that increase the production and volume of urine. This class of drugs achieves this objective primarily by suppressing receptors that aid in the reabsorption of Na+, the most abundant extracellular cation, from the renal tubules, thereby increasing the osmolality of the renal tubules and consequently suppressing water reabsorption. Osmotic diuretics cause a direct increase in luminal hyperosmolarity in the renal tubules without affecting electrolyte balance, whereas aquaretics are substances that act directly by only affecting the excretion of water.[4][5]
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This comprehensive review addresses all the relevant aspects of diuretic therapy, emphasizing the understanding of the basic pharmacophysiological mechanisms of drug action and that of adverse effects but also to more pragmatic aspects of dosing. Diuretics fall into several classes and subcategories depending on their mechanism and site of their action along the nephron. The classification is presented in Table 1, which lists all the available individual drugs in all the different classes, their peculiarities, chemical nature, their major site of action along the nephron, diuretic target molecule, and the percentage of Na+ reabsorption blocked.[6][7][8] Additionally, Table 1 also gives information (to put things in a broader perspective) about miscellaneous agents that do not have a conspicuous diuretic action and are not used for diuresis, but they do have some diuretic effect which is noticeable which must be taken into account during therapy with these agents.
Indications
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Diuresis is necessary for a variety of non-edematous and edematous conditions, which require clearing out excess water when the body abnormally sequesters fluid in the third space in the form of edema. Indications for each individual drug are given below in tables 2 through 5. The quintessential of edematous conditions is heart failure (HF), where the inefficiency of the heart’s pumping ability results in:
1. Decreased renal perfusion leading to activation of the renin-angiotensin-aldosterone-system (RAAS) and
2. Long-standing venous stasis leading to extravasation of fluid into the interstitial space, both of which lead to intravascular volume expansion and result in signs of congestion such as weight gain, dyspnea, and generalized edema.[9]
Pulmonary edema, most commonly resulting from HF, is also an indication for diuretic use. Loop diuretics (due to their greater effectiveness) are the cornerstone of diuretic therapy in symptomatic HF, with furosemide being the most widely used loop diuretic (albeit Torsemide with better pharmacological properties remains underexploited and a comparison trial, TRANSFORM-HF, is currently underway) according to both New York Heart Association (NYHA) and European Society of Cardiology (ESC). These agents are started at lower doses, titrated upwards, and monitored through urine output and body weight measurements. The addition of thiazide diuretics (metolazone, hydrochlorothiazide) to loop diuretics can help relieve symptoms when loop diuretics are not sufficient in HF, as detailed below in the administration section. Aldosterone receptor antagonists (ARA) reduce the mortality and morbidity of advanced systolic HF and patients with ejection fraction less than 35% falling into NYHA-HF classification categories II-IV. This effect is because aldosterone escapes suppression on chronic use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), whereas the addition of ARAs can protect from the effects of aldosterone in such patients.[10][11][12]
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Diuretics, along with salt restriction, are also recommended as the first-line therapy in ascites due to liver cirrhosis.[13] In cirrhotic ascites, spironolactone is the drug of choice for initial therapy (due to its antiandrogenic effect), although a loop diuretic may be added as an adjunct if the treatment fails or can be added at the outset in synergistic combination therapy.[14][15] In both HF and cirrhosis, renal dysfunction contributes to the pathophysiology through further activation of RAAS to increase fluid retention.[16][17] Fluid overload that develops in renal insufficiency or acute kidney injury patients increases mortality, and loop diuretics are the favored initial therapy in these patients though renal replacement therapy is the long-term solution.[18][19] Nephrotic syndrome (NS), characterized by hypoalbuminemia, proteinuria, and hyperlipidemia, is an edematous condition that requires diuretic therapy.[18] Activation of epithelial Na+ channels (ENaCs) in the collecting ducts is the mechanism of edema formation in NS, while RAAS activation could also play a minor role. All the diuretics are serum albumin-bound, and hence hypoalbuminemia in NS decreases the load of diuretic delivered to the renal tubules. Co-administration of albumin with furosemide or a combination of furosemide and ENaC inhibitor such as triamterene has shown some success in kidney disease patients with hypoalbuminemia.[20][21] A gain-of-function mutation in ENaC receptors clinically causes Liddle syndrome, for which ENaC inhibitor amiloride is the treatment of choice.[22]
Thiazides are the best first choice for hypertension, as concluded in a recent Cochrane review, and chlorthalidone is the best first-line agent among all the anti-hypertensive compared according to the 2017 American college of cardiology (ACC) hypertension guidelines.[23][24] Chlorthalidone, with its longer duration of action and longer half-life at lower doses, was found to significantly reduce the risk of cardiovascular (CV) events when compared to other anti-hypertensive medications. Indapamide has lower metabolic adverse effects when compared to chlorthalidone due to its non-interference in lipid or glucose metabolism and much safer for use in hypertension, making it suitable for patients with diabetes. Direct vasodilatory effects of thiazide-like diuretics also contribute to lowering blood pressure (BP) on long-term therapy. On the other hand, loop diuretics may be the preferred agent when hypertension is associated with chronic kidney disease (CKD) or glomerular filtration rate (GFR) less than or equal to 30 mL/min (though some recent reports still favor thiazides in this setting) and potassium-sparing diuretics (PSD) are used in hypertensive patients with K+ or Mg2+ loss.[25][26][27][28][29]
Thiazide-related reabsorption of calcium might be advantageous in nephrolithiasis and hypercalciuria, whereas loop diuretics cause calciuresis and therefore are suitable for use in symptomatic hypercalcemia patients.[30][31] Diabetes insipidus, a polyuric disease, results in a loss of dilute urine with low sodium levels, and paradoxically thiazide diuretics can help by increasing distal tubule Na+ excretion, which compensatively increases water and Na+ reabsorption in the proximal tubule (PT); thus impairing the maximum diluting capacity of kidneys.[32][33] Acetazolamide, the only carbonic anhydrase inhibitor available, induces metabolic acidosis by increased bicarbonate excretion and is used as a prophylaxis in high altitude sickness where it counteracts the hypoxia-induced respiratory alkalosis raising the PaO2. With similar logic, its use is warranted in reversing metabolic alkalosis.[34] Acetazolamide effectively reduces the intraocular pressure and is used for short-term therapy for open-angle glaucoma when topical therapy is not feasible.[35] There is inconclusive evidence “for” or “against” the use of diuretics in Ménière disease.[36]
Osmotherapy is the mainstay of medical therapy for raised intracranial pressure (ICP) after traumatic brain injury and cerebral edema. Hyperosmolar therapy with mannitol reduces elevated ICP rapidly in less than an hour though a rebound (an initial increase of ICP) is possible. Mannitol also promotes diuresis in acute renal failure and excretion of toxic metabolites and substances. Though hypertonic saline similarly is used to treat high ICP and sometimes has demonstrated greater efficiency than mannitol is not considered a diuretic.[37][38]
Diuretics can also be employed less commonly in the active elimination of toxic substances by forced diuresis, which increases urine volume per unit time. Clinicians employ loop diuretics along with alkalinization of the urine in forced alkaline diuresis in the treatment of salicylate, phenobarbital, and lithium poisoning.[39][40] Loop diuretics (along with salt tablets) are also used as a second-line therapy to decrease urine concentration in the syndrome of inappropriate antidiuretic hormone secretion (SIADH), where the mainstay of therapy is the restriction of water intake.[41] The loop diuretic bumetanide has shown effectiveness as an anti-seizure drug. It is used in temporal lobe epilepsy in addition to other central nervous system pathologies such as autism and schizophrenia.[6]
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